Genetic interactions between CSAS and voltage-gated ion channel genes. A, CSAS and para show strong synergistic interactions. TS-paralysis assays of flies with different combinations of CSAS and para mutant alleles. Whereas heterozygous para mutations do not have TS paralysis, they significantly exacerbate the paralysis defect of CSAS mutants. This synergistic enhancement of the phenotype is rescued by a para genetic duplication (paraDp). The presence of three copies of normal para locus (para+/+/Dp) can ameliorate the phenotype of CSAS mutants even further. parats1/+ and paraLk5/+, heterozygotes for para TS and null alleles, respectively; CSASMi/Mi, CSAS homozygous mutant; parats1/+
CSASMi/Mi and paraLk5/+
CSASMi/Mi, combinations of two different para heterozygous alleles with CSASMi homozygote; paraLk5/+/Dp
CSASMi/Mi, combination of para heterozygous null allele, para duplication, and CSASMi homozyous mutant; para+/+/Dp
CSASMi/Mi, combination of para homozygous wild-type allele, para duplication, and CSASMi homozyous mutant. At least 20 five-day-old female flies were assayed for each genotype. Statistical analysis was performed using one-way ANOVA followed by multiple-comparison Wilcoxon each pair test. *p < 0.05 and ***p < 0.001, statistically significant differences. B, CSAS and sei exhibit genetic interactions while alleviating each other's paralysis phenotype. TS-paralysis assays of single and double mutants for CSAS and sei. Adding a single mutant allele of CSAS to seits1 homozygotes significantly diminishes their TS-paralysis phenotype. A heterozygous seits1 mutation has a similar effect on CSAS homozygous mutants. At least 20 five-day-old flies were assayed for each genotype. Compared genotypes represent siblings obtained from the same parents. t test, **p < 0.01, statistically significant differences. Error bars are SEM.